methyl mercury neurons
The dose-dependent toxic effect of methyl mercury on neurons.

Andrew Hall Cutler, a Princeton chemical engineer, emphasized the evidence linking mercury poisoning to Parkinson’s Disease, even citing the 9th ed. of Merritt’s Textbook of Neurology that, as clinical protocol, mercury toxicity should be considered as an alternative diagnosis for Parkinson’s patients. I wonder how many times that has ever actually occurred.

“[The textbook authors] even go so far as to say that the amount of mercury in the brain is not reflected by blood and urine levels. But they don’t say HOW to tell if mercury is the problem so MD’s continue to hold a religious belief that nobody gets mercury tox except at work, and that urine levels below extremely high amounts exclude it. 

“The symptoms of mercury intoxication are extremely close to those of Parkinson’s disease if you read places that describe real patients …

Some of the unexplained biochemical abnormalities in Parkinson’s are commonly observed among mercury tox patients by alternative practitioners. For example, patients with Parkinson’s and motor neuron diseases often have elevated plasma cysteine and reduced sulfate levels, which is observed in about half of mercury toxic individuals.”
—Andrew Hall Cutler, Re: Parkinson’s (2000)

Composite images of ß-tubulin (green) and Hoechst (blue), with the analysis traces shown for the control cells and the cells treated with selected compounds. (Sirenko, 2017)

Mercury induces neurite degeneration, deranges neuronal calcium homeostasis with associated glutaminergic excitotoxicity (Liu, et al., 2014), and inhibits dopaminergic neurotransmission (Götz, et al., 2002; Dreiem, et al., 2009; Blandini, 2010), overlapping with the established pathophysiology of Parkinson’s disease (Masato, et al., 2019). In addition to being induced by pesticides (Singh, et al., 2007), opioids, lead, and traumatic brain injury, there is indeed published evidence of mercury-induced Parkinson’s (Ngim and Devathasan, 1989; Miller, et al., 2003; Ciordia, et al., 2009; Caudle, et al., 2012; Shribman, et al., 2013), and even of clinical improvement of Parkinsonism with chelation therapy (Hryhorczuk, et al., 1982; Finklestein, et al., 1996). These doctors used penicillamine, but I think Cutler’s protocol, involving pharmacologically-timed dosing of alpha-lipoic acid, is the safest and probably only way to completely cure mercury poisoning. 

A retrospective study in Taiwan found that people with amalgam fillings were 1.6 times more likely to get Parkinson’s than those without them (Hsu, et al., 2016). The FDA, Mayo Clinic, World Health Organization, American Dental Association Council on Scientific Affairs, and Scientific Committee on Emerging and Newly Identified Health Risks have all declared amalgam-mercury fillings safe based on “the evidence”, but the clear biochemical evidence, and autopsies of people with dental-amalgam having 2-12 times more mercury in their tissues than normal, illustrate their immense danger. It’s proven that the mercury in amalgam fillings dissolves long-term to release mercury vapors (Chew, et al., 1991), and the inhaled vapors experimentally caused pathological brain changes in animals in just 14 days, in doses analogous to what humans with amalgam fillings are inhaling.

“The average mercury level in the brain of EU citizens with more than 12 amalgalm fillings was 300 ng HG/g brain tissue, well above mercury levels proven to be toxic in vitro on neurons (0.02-36mg Hg/g)”

“Maternal amalgam fillings lead to a significant increase of mercury levels in fetal and infant body tissues including the brain. Placental, fetal and infant mercury body burden correlates with the number of amalgam fillings of the mothers.

“Mercury levels in amniotic fluid and breast milk also significantly correlate with the number of maternal amalgam fillings” (Mutter, 2011).

After mercury vapor (Hg0) is inhaled from amalgam fillings, it easily enters our cells and concentrates in fatty tissues like the brain due to its lipophilicity (“fat-loving” properties). Our body then oxidizes it into Hg++, whose positive charge causes it to covalently bond with other atoms and molecules like proteins. Then it’s no longer lipophilic and can’t easily cross cell membranes to exit, so it stays around essentially permanently, with the brain half-life estimated to be 27.4 years based on autopsies of the brains of poisoned primates (Rooney, 2014). The reason Cutler’s protocol can resolve this is because it carefully manipulates the biochemical properties of those Hg++ atoms using alpha-lipoic acid to slowly pull them out of cells for excretion. 

I think, given instances where a degenerative illness like Parkinson’s is caused by mercury, that protocol is a viable shot at a reversal and cure.

Apparently, all of these bureaucratic councils charged with protecting the population from poisons haven’t adequately looked at the body of evidence they are claiming proves the safety of amalgam fillings, or they’re just incompetent, or a bunch of criminals, but it’s probably a mixture of all three.

Works Cited

Caudle, W. Michael, et al. “Industrial Toxicants and Parkinson’s Disease.” NeuroToxicology, vol. 33, no. 2, 2012, pp. 178–188., doi:10.1016/j.neuro.2012.01.010.

“Chronic Parkinsonism Secondary to Intranasal Administration of a Product of Meperidine-Analogue Synthesis.” New England Journal of Medicine, vol. 310, no. 5, 1984, pp. 325–325., doi:10.1056/nejm198402023100519.

Ciordia, R., et al. “P1.074 Frontotemporal Dementia and Parkinsonism in a Patient with a Chronic Mercury Intoxication.” Parkinsonism & Related Disorders, vol. 15, 2009, doi:10.1016/s1353-8020(09)70196-8.

Cutler, Andrew Hall. Amalgam Illness – Diagnosis and Treatment What You Can Do to Get Better ; How Your Doctor Can Help You. 1999.

Diansari, Viona, and Ellyza Herda. “Mercury Releasing from Amalgam with Disinfectan Solution.” Padjadjaran Journal of Dentistry, vol. 20, no. 3, 2008, doi:10.24198/pjd.vol20no3.14127.

Dreiem, Anne, et al. “Methylmercury Inhibits Dopaminergic Function in Rat Pup Synaptosomes in an Age-Dependent Manner.” Neurotoxicology and Teratology, vol. 31, no. 5, 2009, pp. 312–317., doi:10.1016/

Dreiem, Anne, et al. “Methylmercury Inhibits Dopaminergic Function in Rat Pup Synaptosomes in an Age-Dependent Manner.” Neurotoxicology and Teratology, vol. 31, no. 5, 2009, pp. 312–317., doi:10.1016/

Farina, M. “Methylmercury Increases Glutamate Release from Brain Synaptosomes and Glutamate Uptake by Cortical Slices from Suckling Rat Pups: Modulatory Effect of Ebselen.” Toxicological Sciences, vol. 73, no. 1, 2003, pp. 135–140., doi:10.1093/toxsci/kfg058.

Götz, M. E., et al. “Methylmercury Induces Neurite Degeneration in Primary Culture of Mouse Dopaminergic Mesencephalic Cells.” Journal of Neural Transmission, vol. 109, no. 5-6, 2002, pp. 597–605., doi:10.1007/s007020200049.

Hryhorczuk, Daniel O., et al. “Treatment of Mercury Intoxication in a Dentist with N-Acetyl-D,L-Penicillamine.” Journal of Toxicology: Clinical Toxicology, vol. 19, no. 4, 1982, pp. 401–408., doi:10.3109/15563658208992494.

Hsu, Yung-Chuang, et al. “Association between History of Dental Amalgam Fillings and Risk of Parkinson’s Disease: A Population-Based Retrospective Cohort Study in Taiwan.” Plos One, vol. 11, no. 12, 2016, doi:10.1371/journal.pone.0166552.

Langston, J., et al. “Chronic Parkinsonism in Humans Due to a Product of Meperidine-Analog Synthesis.” Science, vol. 219, no. 4587, 1983, pp. 979–980., doi:10.1126/science.6823561.

Liu, Wei, et al. “Excitotoxicity and Oxidative Damages Induced by Methylmercury in Rat Cerebral Cortex and the Protective Effects of Tea Polyphenols.” Environmental Toxicology, vol. 29, no. 3, 2012, pp. 269–283., doi:10.1002/tox.21755.

Masato, Anna, et al. “Impaired Dopamine Metabolism in Parkinson’s Disease Pathogenesis.” Molecular Neurodegeneration, vol. 14, no. 1, 2019, doi:10.1186/s13024-019-0332-6.

Miller, Krzysztof, et al. “Parkinsonism in Chronic Occupational Metallic Mercury Intoxication.” Neurologia i Neurochirurgia Polska, U.S. National Library of Medicine, 2003,

Moretto, A., and C. Colosio. “Biochemical and Toxicological Evidence of Neurological Effects of Pesticides: The Example of Parkinson’s Disease.” NeuroToxicology, vol. 32, no. 4, 2011, pp. 383–391., doi:10.1016/j.neuro.2011.03.004.

Ngim, Chun-Han, and Gobinathan Devathasan. “Epidemiologic Study on the Association between Body Burden Mercury Level and Idiopathic Parkinson’s Disease.” Neuroepidemiology, vol. 8, no. 3, 1989, pp. 128–141., doi:10.1159/000110175.

Owens, W E. “Dystonia, Tremor, and Parkinsonism in a 54 Year Old Man with 2-Hydroxyglutaric Aciduria.” Journal of Neurology, Neurosurgery & Psychiatry, vol. 75, no. 9, 2004, pp. 1362–1363., doi:10.1136/jnnp.2003.033571.

Parkinson, J. “An Essay On The Shaking Palsy.” Archives of Neurology, vol. 20, no. 4, 1969, pp. 441–445., doi:10.1001/archneur.1969.00480100117017.

Rasheed, Mohd Sami Ur, et al. “Coherent and Contradictory Facts, Feats and Fictions Associated with Metal Accumulation in Parkinson’s Disease: Epicenter or Outcome, Yet a Demigod Question.” Molecular Neurobiology, vol. 54, no. 6, 2016, pp. 4738–4755., doi:10.1007/s12035-016-0016-y.

Rokad, Dharmin, et al. “Role of Neurotoxicants and Traumatic Brain Injury in α-Synuclein Protein Misfolding and Aggregation.” Brain Research Bulletin, vol. 133, 2017, pp. 60–70., doi:10.1016/j.brainresbull.2016.12.003.

Rooney, James P.k. “The Retention Time of Inorganic Mercury in the Brain — A Systematic Review of the Evidence.” Toxicology and Applied Pharmacology, vol. 274, no. 3, 2014, pp. 425–435., doi:10.1016/j.taap.2013.12.011.

Shribman, Sam, et al. “Heavy Metal Toxicity: Lessons From A Case Of Simultaneous Occupational Exposure To Manganese And Mercury.” Journal of Neurology, Neurosurgery & Psychiatry, vol. 84, no. 11, 2013, doi:10.1136/jnnp-2013-306573.126.

Singh, C, et al. “Pesticides and Metals Induced Parkinson’s Disease: Involvement of Free Radicals and Oxidative Stress.” Cellular and Molecular Biology (Noisy-Le-Grand, France), U.S. National Library of Medicine, 30 May 2007,

Teixeira, Francisco B., et al. “Exposure to Inorganic Mercury Causes Oxidative Stress, Cell Death, and Functional Deficits in the Motor Cortex.” Frontiers in Molecular Neuroscience, vol. 11, 2018, doi:10.3389/fnmol.2018.00125.

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